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Hematology > 6: Anticoagulants, Thrombolytics, Antiplatelet agents & Antifinrinolytics > Flashcards

6: Anticoagulants, Thrombolytics, Antiplatelet agents & Antifinrinolytics Flashcards

0
Q

What rae Thrombolytics/Fibrinolytic’s?

A

Substances that promote the destruction of already formed blood clots or thrombi (i.e lyse thrombi) by disrupting the fibrin mesh

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1
Q

What are Anticoagulants?

A

Substances that prevent the synthesis of a fibrin network which inhibits coagulation and the formation of thrombi.

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2
Q

What are Anti platelets?

A

Drugs that reduce the adhesion and aggregation of platelets

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3
Q

What are Antifibrinolytics?

A

Drugs that promote the formation of clots and prevent excessive bleeding

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4
Q

What do Anticoagulants inhibit?

A

The action or formation of one or more of the clotting factors

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5
Q

Why should Anticoagulants be treated with caution?

A

They create an immediate defect (minutes when given IV, hours when given orally) in the clotting mechanism and should be treated with caution.

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6
Q

What is the range between sufficient therapy and hemorrhagic risk?

A

The risk is narrow and varies considerably from patient to patient.

  • A large # of unrelated drugs also affect the dose of the anticoagulant needed to produce a desired effect.
  • Individual treatment & frequency lab tests are imperative.
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7
Q

What are the Anticoagulants be divided into?

A

1) Indirect Thrombin Inhibitors (basically HEPARIN :)
2) Coumarin Anticoagulants (basically WARFARIN)
3) Direct THROMBIN INHIBITORS
4) DIRECT FACTOR X INHIBITORS

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8
Q

What is Heparin ?

A

Commercial heparin is actually a mixture of heparins (protein molecules) w/ a wide range of molecular weights

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9
Q

What are the 2 MOST common preparations:

A

1) Unfractionated heparin (UFH)–Heparin Sodium

2) Low-molecular-wt heparin (LMWH)– Fragmin, Innohep, Lovenox

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10
Q

How does Heparin work ?

A

Heparin stimulates Antithrombin III (this neutralizes the activity of factor & other factors)

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11
Q

What occurs to the intrinsic system without factor Xa?

A

Prothrombin can’t be converted into thrombin, which ultimately prevents FIBRIN formation from FIBRINOGEN

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12
Q

Why is Heparin called an “indirect thrombin inhibitor” ?

A

Stimulates heparin cofactor II which inhibits thrombin

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13
Q

What is Unfractionated Heparin (UFH)

A

**Effective parenteral ANTICOAGULANT for the PREVENTION of clots!

-Discovered in 1916 and has been used for more than 50 years

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14
Q

Why is Unfractionated Heparin (UFH) not effective if given orally?

A

Not absorbed if given orally as heparin proteins are destroyed by stomach acidity.

***Given by IV (bolus or infusion)

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15
Q

When UFH binds to a number of plasma proteins (or endothelial cells & macrophages) what happens?

A

It reduces its anticoagulation activity & causes a rather larger variability of anticoagulant response among patients.

***The relationship between UFH dose & UFH response is a bit tricky

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16
Q

Since the anti-coagulant response to UFH varies among patients what is it important to do?

A

It is standard practice to adjust the dose of UFH & monitor its clinical effectiveness w/ the activated partial thromboplastin time (APTT)

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17
Q

What is the normal APTT time?

A

25-36 seconds

**Therapeutic levels of UFH will typically prolong the aPTT (activated partial thromboplastin time) to 2-2.5 times that of the normal value

18
Q

How can LMWH preparations be used?

A

In-hospital or out-of-hospital setting b/c they can be administered SC(typically w/ pre-filled needle/syringe systems) on a body weight basis w/out the needle for lab monitoring

19
Q

What is the only major coumarin anticoagulant in the US?

A

Warfarin (Coumadin)

**Can lead to death by hemorrhage or internal bleeding

20
Q

How does Warfarin work?

A

Inhibits blood clotting mechanisms by interfering w/ the hepatic synthesis of the VITAMIN K DEPENDENT CLOTTING FACTORS (2, 7, 9, 10)

21
Q

What is the long-term treatment or prophylaxis of Warfarin?

A

1) Venous thrombosis
2) PE

*Post-MI and post-op (after cardiac, vascular surgery) patients. Prevention of systemic thromboembolism in patients w/ prosthetic heat valves or atrial fibrillation

22
Q

What is INR?

A

The therapeutic range for oral anticoagulation therapy is defined in terms of the international normalized ration (INR)

*****Therapeutic levels of warfarin should be adjusted to achieve an INR of 2.0-3.0

23
Q

What are the Key Drug-Drug Interactions Warfarin that inhibit warfarin metabolism(inhibit breakdown) ?

A

These inhibit warfarin metabolism:

1) Cimetidine (Tagamet) –acid reflux
2) Acetaminophen (Tylenol)
3) High dose, acute alcohol

***Keeps it around in the blood longer :)

24
Q

What are the Key Drug-Drug Antibiotic Interactions that inhibit warfarin metabolism (inhibiting its breakdown)?

A

1) Azithromycin (Zithromax)
2) Ciprofloxacin
3) Clarithromycin
4) Erythromycin

***INR goes up!! (when inhibited) and can lead to bleeding.
(Sticks around a lot long and accumulated in the body)

25
Q

How can synthetic thyroid hormones affect the catabolism of many clotting factors & can potentiate the effects of warfarin?

A

INCREASE ( inhibit the anticoagulant action-blood clots)

26
Q

Which Drugs stimulate WARFARIN metabolism (breaking it down fast) and may diminish the desired effects?

A

1) Chronic alcohol use
2) Phenytonin (Dilantin) –seizure meds

***Oral contraceptives INCREASE the synthesis of many factors and can reduce the effects of warfarin (causes blood clots)

Note: Rhis DECREASES the INR !!

27
Q

What does interactions involving warfarin & food rich in vitamin K result in?

A

DECREASED warfarin effects by stimulating the synthesis of vitamin K dependent clotting factors.

***Often b/c of leafy vegetables (maintain consistent daily intake)

28
Q

What are Warfarin overdoses typically treated by?

A

With vitamin K & transfusion

29
Q

What are the side effects of Warfarin?

A

Bleeding is most common side effect. Occurs most often from the mucous membranes of the GI tract & the genitourinary tract.

30
Q

Why is Warfarin contraindicated during pregnancy (Category X) ?

A

Should not be used during pregnancy b/c it crosses the placenta & is teratogenic.

***Breast feeding should also be avoided during warfarin therapy!!

31
Q

What are the Direct Thrombin Inhibitors?

A

Example: Dabigatran (Pradaxa) 1st orally direct thrombin inhibitor!!!

If offers an alternative to warfarin as an orally administered anticoagulant.

**This NEW drug does not require frequent blood tests for INR, doesn’t affect vitamin K or antibiotic levels :) :)

32
Q

What is an example of a DIRECT FACTOR X INHIBITORS?

A

Xarelto

newly release in 2011

33
Q

What are Thrombolytics/Fibrinolytics?

A

Rapidly lyse thrombi when administered intravenously by catalyzing the formation of plasmin from plasminogen

**Bust clot to regulate regular blood flow

34
Q

What are examples of Thrombolytics/Fibrinolytics?

A

1) Streptokinase
2) Urokinase
3) Synthetic tPA
4) Others

35
Q

Why would you administer Thrombolytics/Fibrinolytics?

A

For acute Mi, acute ischemic stroke and PE.

***for best results, Thrombolytics work best the sooner they are initiated from the onset of the event.

36
Q

What are the main classes of Antiplatelet agents?

A

1) Cyclooxygenase Inhibitors( aspirin)
2) Thienopyridines (ADP Inhibitors)
3) GP IIb/IIIa inhibitors

37
Q

How does Aspirin act on platelets?

A

By inhibiting the synthesis of TXA2 one of the substances that helps make the platelets sticky & more likely to aggregate

38
Q

What are the Thienopyridines (ADP Inhibitors?)

A

Prevent the binding of ADP to its receptor on platelets, thereby inhibiting an important pathway that leads to platelet aggregation.

39
Q

What is the main drug that fits in this category ( Thienopyridines (ADP Inhibitors?)

A

CLOPIDOGREL (PLAVIX)

or new one Effient (ADP inhibitor)

40
Q

What are GP IIb/IIIa inhibitors?

A

These inhibit the activation of glycoproteins IIb/IIIa receptors on platelets, inhibiting the “final common pathway” for platelet aggregation

41
Q

What is an example of a drug that is an GP IIb/IIIa inhibitors?

A

ABCIXIMAB (REOPRO)

**Administered IV w/ an initial bolus followed by constant infusion

42
Q

What are Antifibrinolytics? What is an example?

A

Inhibits the activation of plasminogen to plasmin
(***Counteracts the Tissue plasminogen activator tPA)

Example= Tranexamic acid (reduce clots from being dissolved, keep them around longer)

43
Q

What is Tranexamic acid used for in dentistry?

A

Used in the form of a 5% mouth rinse after extractions or surgery in patients w/ prolonged bleeding time, e.g from acquired or inherited disorders

**PROMOTES CLOTS

Hematology (8 decks)

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